Location of tumour necrosis factor alpha by immunohistochemistry in chronic inflammatory bowel disease.

Simon Murch, Christian Braegger, J A Walker‐Smith, Thomas T. MacDonald

Gut · 1993 · 525 citations · 45 references

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TL;DR

This study mapped the location and density of TNF‑α–positive cells in intestinal biopsies from 24 chronic inflammatory bowel disease patients (15 Crohn’s disease, 9 ulcerative colitis) and 11 controls using immunohistochemistry. TNF‑α–positive cells were markedly increased in the lamina propria of both Crohn’s disease and ulcerative colitis, with ulcerative colitis showing subepithelial macrophage dominance and Crohn’s disease exhibiting an even lamina propria distribution plus submucosal clustering around vessels, suggesting that TNF‑α contributes to epithelial and endothelial damage, inflammatory cell recruitment, and prothrombotic effects in both conditions.

Abstract

This study determined the location and tissue density of cells immunoreactive for tumour necrosis factor alpha (TNF alpha) in intestinal specimens from 24 patients with chronic inflammatory bowel disease (15 with Crohn9s disease, nine with ulcerative colitis) and 11 controls. There was significantly increased density of TNF alpha immunoreactive cells in the lamina propria of both ulcerative colitis and Crohn9s disease specimens, although the distribution of these cells differed in the two conditions. In ulcerative colitis most of the TNF alpha immunoreactivity was seen in the subepithelial macrophages, with comparatively less in the deep lamina propria, while in Crohn9s disease immunoreactive cells were distributed evenly throughout the lamina propria. Increased submucosal immunoreactivity was found only in Crohn9s disease, in which TNF alpha positive macrophages tended to cluster around arterioles and venules, often infiltrating and disrupting vascular endothelium. It is suggested that this degree of TNF alpha production probably contributes significantly to the pathogenesis of both Crohn9s disease and ulcerative colitis, by impairing the integrity of epithelial and endothelial membranes, increasing inflammatory cell recruitment, and by prothrombotic effects on the vascular endothelium.

References

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